A. Introduction. Respiratory failure is a common admitting diagnosis in the hospital and intensive care unit (ICU). There are two underlying mechanisms of respiratory failure.
a. Failure to oxygenate. The patient’s PaO2 is less than 60 mm Hg while breathing room air.
b. Failure to ventilate. The patient’s PaCO2 is greater than 50 mm Hg.
B. Causes of Respiratory Failure
a. Failure to oxygenate (see Chapter 17). Of the following five mechanisms of hypoxemia, the last two rarely cause respiratory failure.
i. Ventilation-perfusion (V/Q) mismatch
1. Diseases of the airways and pulmonary vasculature (e.g., chronic obstructive pulmonary disease (COPD), asthma, pulmonary embolism) may manifest as hypoxemia through a pure V/Q mismatch mechanism. These will always correct with 100% FiO2.
2. Alveolar filling diseases (e.g., acute respiratory distress syndrome [ARDS], pneumonia) usually cause hypoxemia through both V/Q mismatch and intrapulmonary shunting. They will not always completely correct with application of 100% Fio2.
iii. Diffusion defect (rarely a cause of acute respiratory failure)
iv. Right-to-left intracardiac shunt
v. Low inspired partial pressure of oxygen
b. Failure to ventilate. Hypercapnia is caused by impaired ventilation. Causes can be broken down into two broad categories: “will not breathe” and “cannot breathe.” The “will not breathe” category points to derangement in the respiratory centers of the brain. “Cannot breathe” is defined as an inability to sustain an adequate minute ventilation (Ve), where Ve = respiratory rate (RR) . tidal volume (Vt) to fully exhale the CO2 produced in the body. Increased dead space and/or increased production of CO2 increase ventilation requirements.
i. “Will not breathe:” central nervous system (CNS) depression, most commonly from drugs (opiates, benzodiazepines, and alcohol), obesity hypoventilation syndrome (OHS), and rarely from brain tumor/stroke.
ii. “Cannot breathe:”
1. Processes that reduce or prevent upregulation of minute ventilation (Ve) and/or increase CO2 production while limiting a compensatory increase in Vt and/or RR.
a. Upper airway obstruction (e.g., epiglottitis, laryngospasm, obstructive sleep apnea).
b. Lower airway obstruction (e.g., asthma, COPD).
c. Lung parenchymal abnormalities (e.g., interstitial fibrosis, pneumonia, congestive heart failure, ARDS).
2. Respiratory muscle weakness: neuromuscular disorders (e.g., botulism, Guillain-Barré syndrome, amyotrophic lateral sclerosis, myxedema), paralyzed or mechanically disadvantaged diaphragm (e.g., phrenic nerve palsy).
3. Chest wall/pleural disorders (e.g., obesity, kyphoscoliosis, large pleural effusions).
4. Dead space ventilation: Pulmonary capillary bed destruction/occlusion (e.g., emphysema, ARDS, pulmonary embolism) can increase dead space ventilation and cause hypercarbia if patient is unable to mount a compensatory increase in minute ventilation.
C. Approach to the Patient
a. Assess the urgency of the situation
i. If respiratory failure is acute, evaluate the patient to determine therapy. The rest of this chapter deals primarily with acute respiratory failure.
ii. If respiratory failure is chronic, there is less urgency to treat, and more time to evaluate the patient is often available.
b. Assess the need for intubation
i. If the patient has any of the following signs, be prepared to intubate:
1. Significantly elevated respiratory rate (>30 respirations/min).
2. Signs of fatigue and labored respiration.
3. Use of accessory muscles to breathe.
4. Stridor (suggests impending upper airway obstruction).
5. Depressed level of consciousness and inability to protect the airway.
ii. Indications for intubation are discussed in Chapter 14. In general, if you think a patient might need to be intubated, you are probably right! It is better to intubate early than to delay or fail to intubate.
c. Attempt to define the cause of the respiratory failure
i. Patient history. Ask about onset, additional symptoms, preceding events, and comorbid conditions.
ii. Physical examination
1. Obtain a full set of vital signs (including oxygen saturation).
2. Note the presence or absence of the following:
a. Alteration in mental status, gag reflex
b. Expiratory wheezes, rales, diminished or absent breath sounds, dullness to percussion
c. Third heart sound (S3) with a sustained point of maximal impulse (PMI), elevated jugular venous pressure, dependent edema (suggestive of congestive heart failure)
d. Abdominal tenderness, bowel sounds
e. Peripheral edema and cyanosis
iii. Diagnostic studies. The following studies should be performed immediately in most patients with acute respiratory failure:
1. Chest radiograph.
2. 12-Lead electrocardiogram (EKG).
3. Arterial blood gas analysis (to assess serum pH, oxygenation [PaO2], and ventilation [PaCO2]). An arterial blood gas is essential to distinguish failure to oxygenate from failure to ventilate:
Low PaO2 → failure to oxygenate
High PaCO2 → failure to ventilate
4. Complete blood count (CBC), serum electrolytes, blood urea nitrogen (BUN), and creatinine.
Suggested Further Readings
Davidson AC, Banham S, Elliott M, et al. BTS/ICS guideline for the ventilatory management of acute hypercapnic respiratory failure in adults. Thorax 2016;71:ii1–ii35.Find this resource:
O’Driscoll BR, Howard LS, Earis J, Mak V. BTS guideline for oxygen use in adults in healthcare and emergency settings. Thorax 2017;72:ii1–ii90.Find this resource: